The role of inflammatory processes in the etiopathogenesis of schizophrenia

In recent years, there has been a growing number of studies trying to explain the role of inflammatory processes in the pathogenesis of mental disorders, including schizophrenia. Epidemiological evidence supports the hypothesis of maternal immune activation during pregnancy, which increases the risk of schizophrenia in the offspring. Studies searching for potential biomarkers for schizophrenia suggest its links with pro-inflammatory cytokines. The process is also linked with complement cascade proteins and microglia cells, although the precise biological underpinnings still remain unclear. Importantly, several clinical trials provide evidence that certain antiinflammatory substances have a beneficial effect on the treatment of schizophrenia. A better understanding of the role of inflammatory processes in the pathogenesis of schizophrenia will enable new solutions in preventive and therapeutic interventions. This paper aims to summarize current evidence on the potential biological mechanisms linking inflammatory processes to the ethiopathogenesis of schizophrenia.